Effect of chronic metabolic acidosis on net electrolyte transport in rat colon

1989 ◽  
Vol 256 (6) ◽  
pp. G1036-G1040 ◽  
Author(s):  
G. M. Feldman
Keyword(s):  
Metabolic Acidosis ◽  
Distal Colon ◽  
Distal Segment ◽  
Proximal Colon ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Chronic Metabolic Acidosis ◽  
In Situ Perfusion ◽  
Arterial Blood ◽  
Acute Correction

Rats fed NH4Cl (5 meq.100 g body wt-1.day-1) for one week developed chronic metabolic acidosis and had an arterial blood pH and plasma HCO3- concentration of 7.27 +2- 0.02 and 16.2 +/- 0.8 meq/l, respectively; control animals had values of 7.36 +/- 0.01 and 22.4 +/- 0.5 meq/l, respectively. Net electrolyte transport was measured in proximal and distal colonic segments by in situ perfusion. In proximal colon, chronic metabolic acidosis increased HCO3- absorption from 3.3 +/- 0.8 to 6.4 +/- 0.6 mu eq.min-1.g-1 but did not alter Na+ absorption. In distal colon, although Na+ transport was unaffected, chronic acidosis reduced HCO3- secretion from -6.9 +/- 0.8 to -4.4 +/- 0.7 mu eq.min-1.g-1 and increased voltage from -18.9 +/- 2.0 to -51.1 +/- 4.2 mV. To evaluate the dependence of these effects on altered arterial pH and HCO3- concentration, NaHCO3 was infused intravenously, raising pH and HCO3- concentration to 7.53 +/- 0.04 and 23.9 +/- 1.7 meq/l, respectively. Although acute correction of chronic metabolic acidosis reduced HCO3- absorption in proximal colon, it did not affect HCO3- secretion or voltage in the distal segment, suggesting that proximal and distal colon respond differently to chronic metabolic acidosis. These results also suggest that chronic metabolic acidosis alters the mechanisms of ion transport in distal colon.

Effect of chronic hypokalemia on H(+)-K(+)-ATPase expression in rat colon

1997 ◽  
Vol 272 (1) ◽  
pp. F22-F30 ◽  
Author(s):  
J. Codina ◽  
T. A. Pressley ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Distal Colon ◽  
Mrna Abundance ◽  
Northern Analysis ◽  
Rat Colon ◽  
Chronic Metabolic Acidosis ◽  
Total Rna ◽  
Alpha Subunits ◽  
Beta Actin ◽  
K Depletion

Although the kidney plays the major role in the regulation of systemic K+ homeostasis, the colon also participates substantively in K+ balance. The colon is capable of both K+ absorption and secretion, the magnitude of which can be modulated in response to dietary K+ intake. The H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase) has been proposed as a possible mediator of K+ absorption in distal colon, but inhibitor profiles obtained in recent studies suggest that two, and perhaps more, distinct H(+)-K(+)-ATPase activities may be present in mammalian distal colon. We have developed highly specific probes for the catalytic alpha-subunits of colonic and gastric H(+)-K(+)-ATPase, alpha 1-Na(+)-K(+)-ATPase, and beta-actin, which were used in Northern analysis of total RNA from whole distal colon and stomach obtained from one of three experimental groups of rats: 1) controls, 2) chronic dietary K+ depletion, and 3) chronic metabolic acidosis. The probe for the colonic but not the gastric H(+)-K(+)-ATPase alpha-isoform hybridized to distal colon total RNA in all groups. A significant increase in colonic H(+)-K(+)-ATPase mRNA abundance was observed in response to chronic dietary K+ depletion but not to chronic metabolic acidosis. The alpha 1-isoform of Na(+)-K(+)-ATPase, which is also expressed in distal colon, did not respond consistently to either chronic dietary K+ depletion or chronic metabolic acidosis. The gastric probe did not hybridize to total RNA from distal colon but, as expected, hybridized to total stomach RNA. However, the abundance of gastric H(+)-K(+)-ATPase or Na(+)-K(+)-ATPase in stomach was not altered consistently by either chronic dietary K+ depletion or metabolic acidosis. Under the conditions of this study, it appears that the mRNA encoding the colonic alpha-isoform is upregulated by chronic dietary K+ restriction, a condition shown previously to increase K+ absorption in the distal colon.

Microradiographic Anatomy of the Explanted Rat Colon

1995 ◽  
Vol 36 (2) ◽  
pp. 210-214 ◽  
Author(s):  
F. Pomerri ◽  
G. Gasparini ◽  
A. Martin ◽  
W. Fries ◽  
E. Pagiaro ◽  
...  
Keyword(s):  
Distal Colon ◽  
Proximal Colon ◽  
Rat Colon ◽  
Sprague Dawley ◽  
Double Contrast ◽  
Colonic Wall ◽  
Sprague Dawley Rats ◽  
Contrast Technique ◽  
Isolated Aorta ◽  
Mucosal Folds

The colon of 32 healthy Sprague-Dawley rats was studied microradiographically. The colonic arterial distribution of 18 rats was examined after injecting barium sulfate into the isolated aorta. The mucosal surface in 9 rats was studied using double-contrast technique after colon explantation. In 5 animals arterial and mucosal studies were carried out simultaneously. The radiographic thickness of the colonic wall was measured using a comparative microscope. The specimens were observed, photographed and examined histologically. Unlike the cecum and distal colon which, when insufflated, do not have mucosal folds, the proximal colon exhibits folds in an oblique direction corresponding to that of the arteries, and the colonic wall in this region is thicker. Comparison between arterial and mucosal microradiographic anatomy and wall thickness enables the proposition of a simple nontopographic division of the rat colon into cecum, proximal colon and distal colon.

Comparison of aldosterone- and RU-28362-induced apical Na+ and K+ conductances in rat distal colon

1994 ◽  
Vol 267 (3) ◽  
pp. G485-G493 ◽  
Author(s):  
R. B. Lomax ◽  
G. I. Sandle
Keyword(s):  
Distal Colon ◽  
Distal Segment ◽  
K Channel ◽  
Rat Colon ◽  
Na Channel ◽  
Channel Blockers ◽  
Mineralocorticoid Antagonist ◽  
Channel Expression ◽  
K Secretion ◽  
Crypt Cells

In mammalian distal colon, aldosterone induces electrogenic Na+ absorption and electrogenic K+ secretion, whereas the sole transport effect of specific glucocorticoid agonists is thought to be stimulation of electroneutral NaCl absorption. In this study, intracellular microelectrodes and Na(+)- and K(+)-channel blockers were used to compare the effects of aldosterone and RU-28362 (a specific glucocorticoid agonist) on apical Na+ and K+ conductances in surface cells and upper crypt cells in the most distal colonic segment from adrenalectomized rats. In control animals, surface cells and crypt cells were devoid of apical Na+ and K+ conductances. In aldosterone-treated animals (70 micrograms.100 g body wt-1.day-1 for 7 days), Na+ conductances were induced in 88% of surface cells but only 40% of crypt cells, and the distribution of K+ conductances was similar (82% of surface cells and 50% of crypt cells). The same dose of RU-28362 also induced Na+ conductances in 82% of surface cells and 50% of crypt cells, which tended to be smaller than those induced by aldosterone. RU-28362, in contrast to aldosterone, had no effect on apical K+ conductance in surface cells or crypt cells. Concurrent treatment with the mineralocorticoid antagonist RU-28318 (3.5 mg.100 g body wt-1.day-1 for 7 days) inhibited Na(+)-channel expression in aldosterone-treated animals but had no effect in RU-28362-treated animals. We conclude that in the most distal segment of rat colon, aldosterone acts via mineralocorticoid receptors to induce apical Na+ and K+ conductances, which are only fully expressed in the surface cell population.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Macromolecular transport across the rabbit proximal and distal colon

Gut ◽  
1999 ◽  
Vol 44 (2) ◽  
pp. 218-225 ◽  
Author(s):  
J A Hardin ◽  
M H Kimm ◽  
M Wirasinghe ◽  
D G Gall
Keyword(s):  
Nervous System ◽  
Small Intestine ◽  
Distal Colon ◽  
Distal Segment ◽  
Proximal Colon ◽  
Colonic Epithelium ◽  
Colonic Tissue ◽  
Ussing Chambers ◽  
Macromolecular Transport ◽  
Energy Dependent

BackgroundAlthough many studies have investigated macromolecular uptake in the stomach and small intestine, little is known about macromolecular uptake in the colon.AimsTo investigate the mechanisms involved in the transport of large antigenically intact macromolecules across the proximal and distal colonic epithelium in the rabbit.MethodsThe mucosal to serosal movement of bovine serum albumin (BSA) was examined in modified Ussing chambers under short circuited conditions. The mucosal surface was exposed to varying concentrations of BSA, and after a 50 minute equilibration period, the mucosal to serosal flux of immunologically intact BSA was determined by ELISA. Total BSA flux was determined by the transport of radiolabelled 125I-BSA.ResultsIntact BSA transport in proximal and distal colonic tissue showed saturable kinetics. Intact BSA transport in the proximal and distal segment was 7% and 2% of the total 125I-BSA flux respectively. Immunologically intact BSA transport in the distal segment was significantly less than that in the proximal segment. Intact BSA transport in the proximal colon was significantly reduced following treatment with sodium fluoride, colchicine, and tetrodotoxin. Cholinergic blockade had no effect on the uptake of intact BSA.ConclusionThe findings indicate that the transport of intact macromolecules across the proximal and distal large intestine is a saturable process. Further, intact BSA transport in the proximal colon is an energy dependent process that utilises microtubules and is regulated by the enteric nervous system.

Effect of the blood lactate concentration on renal glutamine metabolism in dogs with chronic metabolic acidosis

1985 ◽  
Vol 63 (12) ◽  
pp. 1570-1576
Author(s):  
Mitchell L. Halperin ◽  
Ching B. Chen ◽  
Surinder Cheema-Dhadli
Keyword(s):  
Metabolic Acidosis ◽  
Blood Lactate ◽  
Filtration Rate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Glutamine Metabolism ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Constant Rate ◽  
Ammonium Metabolism

It appears that glutamine and lactate are the principal substrates for the kidney in dogs with chronic metabolic acidosis. Accordingly, the purpose of this study was to determine if a higher or lower rate of renal lactate extraction would influence the rate of glutamine extraction at a constant rate of renal ATP turnover. The blood lactate concentration was 0.9 ± 0.01 mM in 15 acidotic dogs. However, eight dogs with chronic metabolic acidosis had a spontaneous blood lactate concentration of 0.5 mM or lower. The kidneys of these dogs extracted considerably less lactate from the arterial blood (19 vs. 62 μmol/100 mL glomerular filtration rate (GFR)). Nevertheless, glutamine, alanine, citrate, and ammonium metabolism were not significantly different in these two groups of dogs. Renal ATP balance in acidotic dogs with a low blood lactate could only be achieved if a substrate other than additional glutamine were oxidized in that segment of the nephron which normally oxidized lactate; presumably a fat-derived substrate and (or) lactate derived from glucose was now the metabolic fuel at these more distal sites. When the blood lactate concentration was greater than 1.9 mM, lactate extraction rose to 219 μmol/100 mL GFR. Glutamine, alanine, citrate, and ammonium metabolism were again unchanged; in this case, ATP balance required substrate flux to products other than carbon dioxide, presumably, gluconeogenesis. It appears that renal ammoniagenesis is a proximal event and is independent of the rate of renal lactate extraction.

31P-NMR in vivo measurement of renal intracellular pH: effects of acidosis and K+ depletion in rats

1986 ◽  
Vol 251 (5) ◽  
pp. F904-F910 ◽  
Author(s):  
W. R. Adam ◽  
A. P. Koretsky ◽  
M. W. Weiner
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Resonance Spectroscopy ◽  
Ph Effects ◽  
Potassium Depletion ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Blood Ph

Renal intracellular pH (pHi) was measured in vivo from the chemical shift (sigma) of inorganic phosphate (Pi), obtained by 31P-nuclear magnetic resonance spectroscopy (NMR). pH was calculated from the difference between sigma Pi and sigma alpha-ATP. Changes of sigma Pi closely correlated with changes of sigma monophosphoesters; this supports the hypothesis that the pH determined from sigma Pi represents pHi. Renal pH in control rats was 7.39 +/- 0.04 (n = 8). This is higher than pHi of muscle and brain in vivo, suggesting that renal Na-H antiporter activity raises renal pHi. To examine the relationship between renal pH and ammoniagenesis, rats were subjected to acute (less than 24 h) and chronic (4-7 days) metabolic acidosis, acute (20 min) and chronic (6-8 days) respiratory acidosis, and dietary potassium depletion (7-21 days). Acute metabolic and respiratory acidosis produced acidification of renal pHi. Chronic metabolic acidosis (arterial blood pH, 7.26 +/- 0.02) lowered renal pHi to 7.30 +/- 0.02, but chronic respiratory acidosis (arterial blood pH, 7.30 +/- 0.05) was not associated with renal acidosis (pH, 7.40 +/- 0.04). At a similar level of blood pH, pHi was higher in chronic metabolic acidosis than in acute metabolic acidosis, suggesting an adaptive process that raises pHi. Potassium depletion (arterial blood pH, 7.44 +/- 0.05) was associated with a marked renal acidosis (renal pH, 7.17 +/- 0.02). There was a direct relationship between renal pH and cardiac K+. Rapid partial repletion with KCl (1 mmol) significantly increased renal pHi from 7.14 +/- 0.03 to 7.31 +/- 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)

Relative effects of systemic pH, PCO2, and HCO3 concentration on colonic ion transport

1984 ◽  
Vol 246 (2) ◽  
pp. G159-G165 ◽  
Author(s):  
A. N. Charney ◽  
L. P. Haskell
Keyword(s):  
Exchange Process ◽  
Respiratory Acidosis ◽  
Distal Colon ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Sodium Absorption ◽  
Sprague Dawley ◽  
Bicarbonate Concentration ◽  
Plasma Bicarbonate ◽  
Blood Ph

To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on colonic electrolyte transport, states of acute metabolic acidosis and alkalosis were created in Sprague-Dawley rats by gavage feeding (NH4)2SO4 and NaHCO3, respectively. During in situ perfusion of the distal colon in pentobarbital-anesthetized animals, electrolyte transport was measured before and after respiratory compensation of the systemic pH. Acute respiratory acidosis and alkalosis also were studied by ventilating animals with 0, 3, or 8% CO2. When animals in all groups were considered, net sodium absorption correlated well with blood PCO2 (r = 0.99) but not with blood pH. Net bicarbonate secretion correlated with the plasma (r = 0.95) and luminal (r = -0.63) bicarbonate concentrations but not with blood pH or PCO2. Net chloride absorption correlated with both blood PCO2 (r = 0.92) and the plasma bicarbonate concentration (r = 0.80). These results suggest that systemic PCO2 affects a sodium chloride absorptive process and that the plasma bicarbonate concentration affects a chloride absorptive-bicarbonate secretory exchange process in the rat colon.

Different types of contractions in rat colon and their modulation by oxidative stress

2001 ◽  
Vol 280 (4) ◽  
pp. G546-G554 ◽  
Author(s):  
Asensio Gonzalez ◽  
Sushil K. Sarna
Keyword(s):  
Potential Role ◽  
Contractile Response ◽  
Circular Muscle ◽  
Distal Colon ◽  
Proximal Colon ◽  
Rat Colon ◽  
Hla B27 ◽  
Different Types

The aim of this study was to investigate the modulation of in vitro rat colonic circular muscle contractions by dextran sodium sulfate (DSS)-induced inflammation and in spontaneous inflammation in HLA-B27 rats. We also examined the potential role of hydrogen peroxide (H2O2) in modulating excitation-contraction coupling. The muscle strips from the middle colon generated spontaneous phasic contractions and giant contractions (GCs), the proximal colon strips generated primarily phasic contractions, and the distal colon strips were mostly quiescent. The spontaneous phasic contractions and GCs were not affected by inflammation, but the response to ACh was suppressed in DSS-treated rats and in HLA-B27 rats. H2O2production was increased in the muscularis of the inflamed colon. Incubation of colonic muscle strips with H2O2suppressed the spontaneous phasic contractions and concentration and time dependently reduced the response to ACh; in the middle colon, it also increased the frequency of GCs. We conclude that H2O2mimics the suppression of the contractile response to ACh in inflammation. H2O2also selectively suppresses phasic contractions and increases the frequency of GCs, as found previously in inflamed dog and human colons.

Cyclic nucleotide-gated cation channels mediate sodium and calcium influx in rat colon

2000 ◽  
Vol 278 (2) ◽  
pp. C336-C343 ◽  
Author(s):  
W. Qiu ◽  
B. Lee ◽  
M. Lancaster ◽  
W. Xu ◽  
S. Leung ◽  
...  
Keyword(s):  
Cyclic Nucleotide ◽  
Calcium Absorption ◽  
Calcium Influx ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Cation Channels ◽  
Rat Colon ◽  
Sodium Absorption

We found mRNA for the three isoforms of the cyclic nucleotide-gated nonselective cation channel expressed in the mucosal layer of the rat intestine from the duodenum to the colon and in intestinal epithelial cell lines in culture. Because these channels are permeable to sodium and calcium and are stimulated by cGMP or cAMP, we measured 8-bromo-cGMP-stimulated sodium-mediated short-circuit current ( I sc) in proximal and distal colon and unidirectional45Ca2+fluxes in proximal colon to determine whether these channels could mediate transepithelial sodium and calcium absorption across the colon. Sodium-mediated I sc, stimulated by 8-bromo-cGMP, were inhibited by dichlorobenzamil and l-cis-diltiazem, blockers of cyclic nucleotide-gated cation channels, suggesting that these ion channels can mediate transepithelial sodium absorption. Sodium-mediated I sc and net transepithelial45Ca2+absorption were stimulated by heat-stable toxin from Escherichia coli that increases cGMP. Addition of l-cis-diltiazem inhibited the enhanced transepithelial absorption of both ions. These results suggest that cyclic nucleotide-gated cation channels simultaneously increase net sodium and calcium absorption in the colon of the rat.

The Effect of Dichlorphenamide on Blood and Cerebrospinal Fluid Acid-Base State in Chronic Ventilatory Failure

1970 ◽  
Vol 39 (3) ◽  
pp. 391-406 ◽  
Author(s):  
D. J. Lane ◽  
J. B. L. Howell ◽  
T. B. Stretton
Keyword(s):  
Metabolic Acidosis ◽  
Linear Relation ◽  
Experimental Studies ◽  
Regulatory Mechanisms ◽  
Acid Base ◽  
Chronic Metabolic Acidosis ◽  
Arterial Blood ◽  
Chest Disease ◽  
Ventilatory Failure ◽  
Arterial Plasma

1. Pco2, [HCO−3] and [H+] have been measured in arterial blood and CSF in twenty-three patients with chronic airways obstruction and five patients without chest disease. 2. Through a range of Pco2 in the CSF from normal to 79 mmHg there was a direct linear relation between Pco2 and [H+]. The slope of this relation (0·41 nmol l−1 mmHg−1) was similar to that reported in experimental studies in animals and would appear to represent the extent to which regulatory mechanisms can protect CSF [H+] against the acidosis of chronic hypercapnia. 3. There was also a direct linear relation between CSF [HCO−3] and arterial plasma [HCO−3], the rise in [HCO−3] in the CSF being less than that in the blood. 4. Thirteen patients were re-studied after receiving the carbonic anhydrase inhibitor dichlorphenamide for 1 week. A metabolic acidosis developed in the arterial blood. In the CSF Pco2 and [HCO−3] fell but [H+] did not change. CSF [H+] is maintained constant and normal in other forms of chronic metabolic acidosis but it seems likely that the constancy observed in the present study was fortuitous. Possible reasons for this are discussed, and it is concluded that variability in responsiveness to ventilatory stimuli between patients is the most likely explanation.

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